The public has been ill-served by journalists reporting on the very real threat that antibiotic resistance poses.

Most accounts describe antibiotic-resistant bacteria as “tough”, “hardy”, “strong” etc. The “superbug” trope itself implies that they have special powers that render them invincible. This isalmostalways untrue.

Resistant bugs, especially multiply-resistant bugs, are generallylessfit/hardy/rugged than their susceptible counterparts. With the exception of community strains of MRSA, they rarely infect or kill otherwise healthy patients. Most cases occur in patients whose health and immune systems have been compromised by other maladies - diabetes, cancer, organ failure. “Superbugs” are not the fierce predators of the microbial world, dauntless killers that take down prime specimens of humanity. Instead they are opportunistic scavengers who pick off the weak and lame - less lion than vulture.

There are no free lunches in biology. Bacteria are relentlessly selected to maximize their own reproduction. Antibiotic resistance is not a character trait like toughness or grit. It results from mutations to genes that have been selected for maximal efficiency over billions of years. Change these genes and you make the bug weaker, not stronger.

The other major source of resistance is acquisition of new genes on mobile genetic elements. At the very least, these new genes require resources that would otherwise go to bacterial reproduction. In both scenarios (mutation or gene acquisition) reproductive efficiency is traded for survival in a very specific environment - that of antibiotic use. In the absence of antibiotics, resistant strains get outcompeted. This general principle has been confirmed repeatedly in lab experiments in which resistant bugs grow more slowly than their susceptible counterparts. I’ve summarized some of these experimentshere.

Antibiotic resistance is not caused by vague, general properties like toughness. It results from specific changes to specific molecules that prevent specific antibiotics from binding specifically to them. Or by the acquisition of genes which code for enzymes that degrade antibiotics. Specifically.

The semi-exception to these rules occurs when antibiotic resistance genes are embedded in clusters of genes on mobile genetic elements. Some of these additional genes encode resistance to other antibiotics, giving rise to multiply-resistant bugs. Other genes may encode resistance to environmental stressors like metals or solvents. Resistance to these stressors often increases resistance to disinfectants. At a superficial level, these bugs do indeed appear “tough” - not killed by antibiotics, not killed by soap or triclosan. Someone who is in a rush to write a clickbait article might not appreciate this distinction between general and specific hardiness. But you have made it through this article, and so you do.

Congratulations, you are now smarter than a science journalist. I leave it to you to decide whether to be elated or relieved.

And if you’ve made it this far, the answer to the original question should be apparent. Vaccines stimulate the immune system to recognize and eliminate bacteria and viruses. A whole different set of molecules are involved. Antibiotic resistance and immune resistance - which is a very real thing, and an interesting topic in its own right - have nothing to do with each other.

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